REVIEW Open Access

Echocardiography in shock managementAnthony S. McLean

Abstract

Echocardiography is pivotal in the diagnosis and management of the shocked patient. Important characteristics inthe setting of shock are that it is non-invasive and can be rapidly applied.In the acute situation a basic study often yields immediate results allowing for the initiation of therapy, while afollow-up advanced study brings the advantage of further refining the diagnosis and providing an in-depthhemodynamic assessment. Competency in basic critical care echocardiography is now regarded as a mandatorypart of critical care training with clear guidelines available. The majority of pathologies found in shocked patientsare readily identified using basic level 2D and M-mode echocardiography. A more comprehensive diagnosis can beachieved with advanced levels of competency, for which practice guidelines are also now available. Hemodynamicevaluation and ongoing monitoring are possible with advanced levels of competency, which includes the use ofcolour Doppler, spectral Doppler, and tissue Doppler imaging and occasionally the use of more recent technologicaladvances such as 3D or speckled tracking.The four core types of shock—cardiogenic, hypovolemic, obstructive, and vasoplegic—can readily be identified byechocardiography. Even within each of the main headings contained in the shock classification, a variety of pathologiesmay be the cause and echocardiography will differentiate which of these is responsible. Increasingly, as a result ofmore complex and elderly patients, the shock may be multifactorial, such as a combination of cardiogenic and septicshock or hypovolemia and ventricular outflow obstruction.The diagnostic benefit of echocardiography in the shocked patient is obvious. The increasing prevalence of critical carephysicians experienced in advanced techniques means echocardiography often supplants the need for more invasivehemodynamic assessment and monitoring in shock.

Keywords: Critical care echocardiography, Shock assessment, Hemodynamic echo evaluation

Abbreviations: 2D, Two-dimensional; AUC, Area under curve; CO, Cardiac output; CSA, Cross-sectional area;ICU, Intensive care unit; IVC, Inferior vena cava; LAP, Left atrial pressure; LVEF, Left ventricular ejection fraction; LVOT, Leftventricular output tract; PAcT, Pulmonary acceleration time; PLR, Passive leg raising; RACE, Rapid assessment by cardiacecho; RAP, Right atrial pressure; SV, Stroke volume; TDI, Tissue Doppler imaging; TEE, Transesphageal echocardiogram;TTE, Transthoracic echocardiogram; VTI, Velocity time integral

BackgroundWhether the cause of shock is unknown, suspected, orestablished, echocardiography is utilized in its diagnosisand management and to monitor progress. It is recom-mended as the modality of first choice in consensus guide-lines [1]. No other investigative bedside tool can offer asimilar diagnostic capability, allowing for exact targetingof the underlying cardiac and hemodynamic problemswhether it be the right heart, left heart, fluid perturba-tions, pericardial, or a cardiac response to vasoplegia as

found in septic shock. The clinician needs to undertake acareful, structured echocardiographic examination, evenin an emergency situation where urgency demands a rapidassessment.Competency standards are well established for both

basic and advanced critical care echocardiography andthe scope of this review will cover both [2, 3] (Table 1).Both transthoracic echocardiography (TTE) and trans-esophageal echocardiography (TEE) expertise should beavailable, the latter being seen as part of the armament-aria of the advanced practitioner. It may be an iterativeprocess whereby a basic assessment or rapid cardiac as-sessment by echo (RACE) is performed immediately inCorrespondence: anthony.mclean@sydney.edu.au

Nepean Hospital, PO Box 63 Penrith, Sydney, NSW 2751, Australia

© 2016 The Author(s). Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, andreproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link tothe Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver(http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

McLean Critical Care (2016) 20:275 DOI 10.1186/s13054-016-1401-7

the deteriorating patient, with subsequent initiation oftreatment, followed at a later time by a more detailedadvanced echocardiographic assessment.

Shock: definition and classificationShock can be defined as a life‐threatening, generalizedform of circulatory failure associated with inadequateoxygen delivery to the cells [1]. The four major under-lying mechanisms, either alone or in combination, in-clude inadequate circulating volume (cardiogenic shock),failure of pump function (hypovolemic shock), obstructionto blood flow (obstructive shock), and loss of vasculartone (vasoplegic shock). The diagnosis of acute circulatoryfailure includes the clinical signs of hypotension (not al-ways present), poor peripheral perfusion determined byskin changes, especially cold, clammy, discolored skin, de-creased urine output (<0.5 ml/kg/min), and altered mentalfunction, including obtundation and confusion. It shouldbe noted that a defined level of blood pressure to denotethe presence of shock is not recommended [1, 4].

Cardiogenic shockCardiogenic shock is the extreme end of the acute deteri-orating heart failure spectrum. A global study involving666 hospitals involving nearly 5000 patients admitted tohospital with acute heart failure found 36 % were first timeepisodes, 37 % were in pulmonary edema, and 12 % werein cardiogenic shock [5]. Overall hospital mortality was12 %, rising to 18 % in those patients admitted to ICU.Cardiogenic shock carries the worst prognosis with im-provements in mortality, from 70 to 50 %, resulting mainly

from early revascularization. Consensus documents frommajor societies are available [6].Although most of the literature pertaining to cardiogenic

shock relates to underlying coronary artery pathology, thecritical care physician encounters a broader range of path-ologies, including sepsis, resulting in severe cardiac failureand echocardiography is the only bedside tool that can ac-curately elucidate the underlying pathology.A RACE assessment, using only two-dimensional (2D)

and M‐mode echocardiography demonstrates majorunderlying abnormalities rapidly in the acute scenario[7]. Overall left ventricular contraction, including ejec-tion fraction, segmental wall motion abnormalities, rightheart failure, clues to intravascular volume status, andpericardial tamponade, can be identified. However, ad-vanced techniques involving the use of spectral Dopplerand tissue Doppler imaging (TDI) yield much more in-formation, providing both diagnostic and hemodynamicevaluation.

Overall cardiac performanceThe estimation of cardiac output by echocardiography(echo) is well validated. Although it can be measuredusing the 2D Simpson’s multidisc method, the use ofpulsed-wave Doppler across the left ventricular outputtract (LVOT) is more accurate [8]. This often supplantsinvasively acquired CO measurements unless continuousmonitoring is considered important. Other parameters ofoverall cardiac function, such as myocardial performanceindex (MPI) and mitral annulus plane systolic excursion(MAPSE) are not well validated in critically ill subjects.The LVOT velocity time integral (VTI) as a single meas-ure that can be used as a surrogate for the stroke volumewith a normal value >20 cm [9]. A value above 18 cm im-plies an adequate stroke volume.

Left ventricular systolic functionContractility is the ability of the myocardium to contractagainst a specific load for any given preload. Echo isused to measure contraction, which is measured as thedegree of myocardial fiber shortening that occurs duringsystole. The most common cause of cardiogenic shockresults from marked reduction in left ventricular con-traction. The size of both the left atrium and ventriclemay provide clues to the duration of the contractile im-pairment, with dilatation indicating a degree of chron-icity (Fig. 1). Left ventricular ejection fraction (LVEF) isa traditional parameter which, though far from ideal, canbe a helpful guide. The Simpson’s multidisc method canbe applied in RACE. Subjective evaluation or “eyebal-ling” the LVEF is reasonably accurate with experiencebut objective measurement should always be consideredin the advanced study. It is sufficiently robust to be usedregularly in large studies in the chronic heart failure

Table 1 Basic and advanced echocardiograph evaluation in theshocked patient

Race Advanced

Modality 2D, M-mode 2D, M-mode

Colour Doppler

Special Doppler

TDI

Assessments LV contraction LV systolic function

RV contraction Diastolic function

Intravascular fluid status RV systolic function

Pericardial tamponade Intravascular fluid status

Valve structure/function

Pericardial tamponade

Hemodynamics

Pulmonary artery pressure

Left atrial pressure

Cardiac output

Ventricular outflow obstruction

LV left ventricle, RACE rapid assessment by cardiac echo, RV left ventricle, TDItissue doppler imaging

McLean Critical Care (2016) 20:275 Page 2 of 10

setting where it serves as a prognostic marker [10].When the endocardial border is difficult to visualize,contrast echo may enhance accuracy [11].Interpretation needs to take into account the effects of

arterial blood pressure (afterload), inotropes, and vaso-pressors. For example, a struggling left ventricle may ap-pear normal in the presence of inotropes. Other cardiacpathologies need to be taken into account as a normalor high LVEF may misled the clinician into believingthere is good cardiac function although marked diastolicor valvular dysfunction is present.Fractional area change (FAC) has been used to assess

the left ventricle with reasonable accuracy in surgical pa-tients undergoing TEE during cardiac surgery [12]. Itcan be measured from either the parasternal short axisview (PSAX) using TTE or the transgastric view withTEE short axis views, using the difference between theend diastolic and end systolic areas divided by the enddiastolic area, with a normal range being 38–60 %. Thereliability is less certain in hemodynamically unstable pa-tients, in the presence of segmental wall motion defectsor left bundle-branch block, or where right ventriculardysfunction exists, and as a result is used less commonlyin the ICU setting compared with the operating theatre.The advanced practitioner can use a number of

Doppler and TDI parameters to more accurately quan-tify left ventricular dysfunction. When mitral regurgita-tion is present, dP/dt can be calculated, a normal valuebeing >1200 mmHg/s and markedly abnormal values be-ing <800 mmHg/s [13]. Using TDI, the myocardial sys-tolic velocity S’, measured from an average of readingsfrom multiple segments, correlates with LVEF. In a study

involving four basal segments, a S’ >7.5 correlated with anLVEF >50 % with a sensitivity of 79 % and specificity of88 % [14]. Using an average of six basal segments, Gulatiand colleagues found an S’ >5.4 indicated an LVEF >50 %with sensitivity 88 % and specificity 97 % [15]. It should benoted that S’ decreases with age and does not differentiateactive contraction from tethering effects.Other techniques currently under investigation, al-

though contributing to left ventricular contraction as-sessment in the stable outpatient population, have yet toprove beneficial in the critically ill. Strain rate imagingand speckle tracking using global longitudinal strainhave been demonstrated to identify systolic dysfunctionin patients with normal LVEF in oncology and heart fail-ure patients [16, 17]. The value in critically ill patients isstill uncertain [18].Any assessment of left ventricular contractility needs

to take the presence or absence of identifiable segmentalwall motion abnormalities into account; if present, ur-gent revascularization should be considered to enhanceprognosis.

Valvular pathologyEchocardiographic investigation extends to possible valvu-lar lesions, both acute and preexisting, like degenerativeaortic stenosis and mitral regurgitation, frequently foundin the older population. Acute lesions such as peri‐infarc-tion rupture of a papillary muscle resulting in severe mi-tral regurgitation may necessitate urgent surgical repair ofthe valve. Initial examination of the valves in the acutesetting, allowing for initiation of treatment, requires rea-sonable but not necessarily expert skills. A more compre-hensive valve examination can be performed later byclinicians highly skilled in valve evaluation (Fig. 2).

Fig. 1 Grossly dilated left ventricle with biventricular pacing wirepresent in right heart in the apical four-chamber view. LV left ventricle,MVmitral valve, RA right atrium, RV right ventricle

Fig. 2 Ruptured mitral papillary muscle post infarction seen by 3Dechocardiography from the apical four-chamber view view. LA leftatrium, LV left ventricle, MV mitral valve

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Left ventricular diastolic dysfunctionApproximately half the patients presenting with acuteheart failure have preserved ejection fraction via anumber of mechanisms, including diastolic dysfunction-reduced coronary flow reserve [19, 20]. High metabolicstates frequently found in critically ill patients can ex-acerbate cardiac failure by worsening diastolic function.Although there is a comprehensive background to asses-sing left ventricular diastolic function, it was the adventof TDI that simplified the situation and brought analysisto the bedside. In particular, TDI analysis of the mitralannulus allows for rapid estimation of left atrial pressure(LAP), an important parameter in evaluating left ven-tricular function and preload.The use of spectral Doppler of mitral inflow still re-

mains paramount. Both an E/A ratio >2 and an E wavedeceleration time <120 ms predict a LAP >20 mmHg[21]. With TDI, the mitral annulus e′ offers a quickguide to the presence of left ventricular diastolic dys-function with a lateral e′ <10 and medial <7 cm/s highlysuggestive of diastolic dysfunction and elevated left atrialpressures [22].The E/e′ ratio, although still affected by loading condi-

tions, is of considerable value by giving a guide to ele-vated left atrial pressures. The original description usingpatients with coronary disease or heart failure used anE/e′ <8 to indicate normal LAP and a value >15 gave anLAP >13 mmHg [23]. The average of the lateral and sep-tal e′ measurements is recommended. Interestingly, re-cent international guidelines on assessing left ventriculardiastolic dysfunction choose a discriminating averageE/e′ value of 14 to identify elevated left atrial pres-sure [24].The E/e′ value used to identify elevated left atrial pres-

sures in patients on positive ventilation is less than thatused in non-ventilated patients, around 12 using theaverage septal/lateral e′ rather than the classic 14–15[25]. However, a precise and accurate value is unclear.Positive pressure ventilation affects left ventricular dia-stolic filling in a number of often opposing ways and theoverall effects are difficult to predict. Increased intratho-racic pressure, by reducing systemic venous return,results in decreased left ventricular preload and, by de-creasing the atrial–ventricular pressure gradient, reducesE and e′. Lung hyperinflation can decrease pulmonaryvascular resistance when the volume increase is less thanthe functional reserve capacity but beyond this will in-crease the resistance with subsequent effects on rightventricular afterload and left ventricular preload. A low-ering of the transmural pressure decreases afterload ofthe left-sided chambers, resulting in an increase in leftatrial contractility and subsequent augmentation of ven-tricular filling, theoretically increasing A and a’, and evenE and e′ [26]. In critically ill patients an E/e′ >13 is

indicative of elevated left atrial pressure and, althoughvery useful, is not without controversy [27, 28].

Other considered pathologies in cardiogenic shockThe contribution of right heart function to shock willbe covered in the “Hypovolemic shock” section. Post-infarction ventricular septal defects, although uncommon,often occur some days after the actual infarction and areusually catastrophic. The presence of new onset aortic re-gurgitation, particularly when it is associated with a peri-cardial effusion, should lead to investigation of dissectionof the thoracic aorta. This requires a TEE.

Hypovolemic shockAlthough particularly pertinent in suspected hypovol-emic shock, assessment of intravascular volume is thestarting point in all types of circulatory failure. Oftenclinically insufficient volume is readily evident but canbe difficult to determine by physical examination alone.At the basic level of competency the clinician relies on2D and M‐mode echocardiography only. When hypovol-emia is severe, 2D views can be impelling when theyshow collapse of the left ventricular walls at end‐systole,the so‐called “kissing walls”. Conversely, fixed bowing ofthe atrial septum into the right atrium throughout thecardiac cycle implies elevated left atrial pressures andfurther fluid is not necessary (Fig. 3). It should be notedthat neither of these signs are specific for intravascularfluid status. Left ventricular end diastolic area (LVEDA)appears to be helpful in assessing response to a volumeload in anaesthetized patients undergoing surgery butunfortunately not in the critically ill patients [29].Inferior vena cava (IVC) variation has been recognized

as a useful parameter for some decades now and, whilefar from ideal, is a good place to start. Numerous studieshave explored refining the technique using vessel diam-eter variation in response to the respiratory cycle, max-imum diameter, and percentage of diameter alteration toassess right atrial pressure (RAP) [30].Guidelines recommend that in the spontaneously

breathing patient an IVC diameter (D) <21 mm that col-lapses with a sniff (i.e., the caval or collapsibility index[CI = (Dmax −Dmin)/Dmax × 100 %]) indicates a normalRAP of 3 mmHg, whereas an IVC diameter >21 mmthat collapses <50 % with a sniff indicates a RAP of>15 mmHg [31]. In a study of 73 emergency patientsover 50 years of age, Nagdev and colleagues demon-strated, without taking IVC diameter into account, thatan IVC collapse of >50 % had a positive predictive valueof 87 % and a negative predictive value of 96 % of a cen-tral venous pressure <8 mmHg with a receiver operatingcurve (ROC) of 0.93 [32]. In a study on IVC diametervariation following fluid administration to hypovolemictrauma patients, inadequate dilatation indicated insufficient

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circulating blood volume despite normalization of bloodpressure [33].The transition from the cardiology setting to critical

care practice resulted in a conceptual change, withchanges in IVC diameter being used to assess fluid re-sponsiveness rather than pressure equivalents.For practical purposes, in the acute setting for the spon-

taneously breathing patient in shock, the IVC diameter ismeasured within 0.5–3 cm from the caval–right atrialjunction in the subcostal view and when the diameter isless than 10 mm the patient is likely to respond to fluid,but when greater than 20 mm that is unlikely. Collapse of>50 % between the diameters of 10–20 mm should resultin a trial of fluid. In the patient on fully supported positivepressure ventilation, the distensibility index (dIVC) is agood guide to fluid responsiveness. The dIVC is calculatedas the ratio of (Dmax−Dmin)/Dmin, with a threshold of 18 %discriminating between responders and non-responderswith 90 % sensitivity and 90 % specificity [34].There are pitfalls when performing IVC measurements

and the operator should take care to obtain a good lon-gitudinal view with the scan plane parallel to the IVCand the probe tilted in both directions to obtain the lar-gest diameter. As the IVC can move inferiorly during in-spiration, two different segments of the vessel can beinadvertently measured using M‐mode, so 2D measure-ments, with the highest possible frame rate, are recom-mended. Neither collapse nor distension of the IVCduring respiratory ventilation should be used on patientsreceiving partial ventilatory support and, even in bothgroups described above, the clinician can only occasion-ally confidently predict fluid responsiveness on the IVCalone. Furthermore, the presence of right heart failure,

increased intra‐abdominal pressure, or pericardial fluidmakes the use of IVC even less reliable.When TEE is being applied, the superior vena cava in

the fully supported ventilated patient can be used and acollapse of >36 % during inspiration discriminates fluidresponders from non‐responders with a sensitivity of90 % and specificity of 100 % [35].The use of static measurements to assess fluid status is

recognized to be inadequate in the majority of situationsand dynamic techniques need to be applied. Administra-tion of a bolus of intravenous fluid, passive leg raising,and positive pressure ventilation-induced variation instroke volume (SV) and CO are commonly employed.As a guide, fluid responsiveness is determined if there is,on average, a >15 % increase in SV or CO. The under-lying physiology is well covered elsewhere and the focusof this review is on the practical application of echocar-diography in shocked patients. [36]. Essentially, large SVvariations occur on the steep part of the Starling curveand small variations on the flat part of the curve and ei-ther the SV or a surrogate measure, such as the velocitytime integral (VTI), can be measured echocardiographi-cally in response to the maneuver chosen. Doppler appli-cation uses the relationship between the velocities ofblood flowing across the LVOT at the level of the aorticvalve annulus or, alternatively, flow across the right ven-tricular outflow tract (RVOT) at the level of the pulmon-ary valve annulus, combined with the cross-sectionalarea (CSA = π(LVOT diameter/2)2) of the chosen loca-tion. CO and SV are measured using pulsed‐waveDoppler with the sample volume placed at the level ofthe aortic annulus for left ventricular outflow (whereSV = VTI × CSA and CO = SV × Heart rate). Care must

Fig. 3 Bowing of interatrial septum from left to right indicating elevated left atrial pressure in PSAX view. AV aortic valve, IAS interatrial septum, LAleft atrium, RA right atrium

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be taken to properly align the Doppler beam to the flowand VTI is measured by tracing the modal velocity.

Selected maneuversIntravenous fluid administrationApplication of a bolus of intravenous fluid has long beenused to assess fluid responsiveness with clinical parame-ters, especially systemic blood pressure, used as an end-point. Pulse pressure variation is used as blood pressuredoes not always reflect fluid responsiveness, particularlywhen other factors, such as impaired left ventricularcontraction or marked vasoplegia, exist. With increasingawareness of the perils of excessive fluid administration,the practice of mini‐boluses of fluid is attractive. This isparticularly the case in patients with impaired left ven-tricular function who are at greater risk of acute pulmon-ary edema. In a study on 39 low volume-ventilatedcritically ill patients, sub-aortic VTI was measured follow-ing an initial 100 ml of starch administered over 1 minutefollowed by another 400 ml over 14 minutes. A change inVTI of >10 % after the first 100 ml predicted fluid respon-siveness with a sensitivity and specificity of 95 % and78 %, respectively (area under curve (AUC) = 0.92) [37].

Respiratory variationDuring the inspiratory phase of positive pressure ventila-tion, right ventricular output is reduced because of a de-crease in venous return (increased intrathoracic pressure)causing a subsequent decrease in left ventricular outputafter two to three beats if both ventricles are volume re-sponsive. These approaches are limited to fully ventilatedpatients and studies were performed using tidal volumesof 8–10 ml/kg. As smaller tidal volumes are not proven tobe diagnostically helpful, it may be necessary to temporar-ily increase these to 8 ml/kg. A SV variation >10 % ishighly predictive of volume responsiveness [38]. An in-crease in a respiratory rate from 14-16 to 30-40 breathsper minute in hypovolaemic patients resulted in a de-crease in pulse pressure variation from 21 % to 4 % and inrespiratory variation in aortic flow from 23 % to 6 %, withno accompanying change in cardiac index [39].One factor to consider when using positive pressure

ventilation to predict fluid responsiveness in mechanic-ally ventilated patients is right ventricular function.Using TDI of the tricuspid annulus, Mahjoub and col-leagues [40] found that an S’ <15 cm/s yields a falsepositive positive pressure ventilation result.

Passive leg raisingPassive leg raising (PLR) has been demonstrated to beapplicable in both spontaneously breathing and venti-lated patients. Correct positioning of the patient is es-sential. CO is measured using pulsed‐wave Doppler. Anincrease in CO or SV of >12 % during PLR was highly

predictive of fluid responsiveness with an AUC of 0.89for the cardiac index and 0.9 for the SV. Sensitivity andspecificity values were 63 and 89 % for CO, and 69 and89 % for SV, respectively [41]. Using esophageal Doppler,Monnet and colleagues [42] demonstrated in 37 venti-lated patients that a PLR increase of >10 % aortic bloodflow predicted fluid responsiveness with a sensitivity of97 % and specificity of 94 %. A false positive response toPLR may occur in the presence of increased intra-abdominal pressure.Assessing intravascular volume should be the first step

in managing all types of shock. A basic approach usingRACE generally identifies gross hypovolemia. Where un-certainty exists about intravascular fluid status, moreadvanced techniques utilizing Doppler and dynamic ma-neuvers should be employed.

Obstructive shockThe common mechanism in patients with obstructiveshock is resistance to blood flow through the cardiopul-monary circulation. Specific pathological diagnoses areacute pulmonary embolus, cardiac tamponade, and dy-namic outflow obstruction; on occasion, it also occurs asa result of a type A dissection of the thoracic aorta or atension pneumothorax. Constrictive pericarditis is a rarecause of obstructive shock.

Acute pulmonary embolusClassic right heart changes identified by echo are diag-nostically and prognostically very helpful, indeed essen-tial, in the shocked patient [43]. Diagnostic criteriainclude dilated right heart chambers, changes in rightventricular contraction, elevated pulmonary artery pres-sures, decreased cardiac output, and intra‐cavity emboli.Dilatation of the right ventricle is readily assessed in theapical four-chamber view with a right ventricle/left ven-tricle area ratio >0.6; gross dilatation is seen with a ratio>1.0. [44]. Right atrial area/volume is best measured bythe Simpson’s method in the apical four-chamber view.Right ventricular contraction can be normal, hyperdy-namic soon after the insult of the pulmonary embolus,or hypodynamic in the later stages. Tricuspid annulusplane systolic excursion (TAPSE) is a reasonably reliableand easily obtainable parameter for overall right ven-tricular contraction with a normal value being >16 mm.TDI, using the lateral tricuspid annulus S’ velocity, is auseful tool to identify early right ventricular dysfunction.A right ventricular S’ velocity <11.5 cm/s predicts rightventricular dysfunction (right ventricular ejection frac-tion <45 %) with a sensitivity of 90 % and specificity of85 % [45]. In regular daily practice an S’ of 10 cm/s is auseful and easily remembered number to differentiatebetween normal and abnormal right ventricular systolicfunction.

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The McConnell sign, where good apical but poor freewall contraction is seen, is considered an important signby some [46]. However, it is also found in right ventricu-lar infarction and its specificity for pulmonary embolismhas been called into question [47, 48]. The pulmonaryartery systolic pressure is most commonly obtained byconverting the peak velocity of the tricuspid regurgita-tion to pressure using the modified Bernoulli equationand adding to the right atrial pressure. Care needs tobe taken to obtain accurate Doppler signals. In theabsence of a reliable tricuspid regurgitant signal, theacceleration time of the pulmonary ejection signal (PAcT)is used [49].As a guide, a PAcT of 70–90 ms indicates a pulmonary

artery systolic pressure of >70 mmHg. The presence ofmid‐systolic notch also indicates severe pulmonary hyper-tension (Fig. 4).The classic 2D sign of pulmonary hypertension result-

ing in a marked increase in right ventricular pressures isparadoxical septal motion, whereby a D‐shaped leftventricle is seen on the parasternal short axis view.The presence of mobile thrombo‐emboli in the rightheart chambers, inferior vena cava, or pulmonary ar-tery are occasionally seen and may push the clinicianto early administration of thrombolytic therapy. Exam-ination of the left ventricle is also informative in severeacute pulmonary embolus, with small chamber size

and reduced cardiac output reflecting reduced leftheart filling.

Cardiac tamponadeWhen the intrapericardial pressure exceeds right heart fill-ing pressure (diastole), impaired filling of the chambersresults in tamponade. A pericardial effusion is usuallyreadily identified by echo, although size is no guide to thepresence of tamponade. Fluid in the pericardial space isgenerally easy to differentiate from a pericardial fat pad ora pleural effusion. The crucial echo findings in RACE es-tablishing the presence of tamponade and the need forrapid drainage are either right atrial wall systolic collapsefor longer than one-third of the cardiac cycle, right ven-tricular wall diastolic collapse, and a dilated IVC [50].Doppler interrogation across the valves by the ad-

vanced user can be used for added diagnostic support.Normal respiratory variation results in an increase of tri-cuspid flow during inspiration and decrease during ex-piration with reciprocal changes occurring with mitralvalve flow. Increases in peak tricuspid velocity are usu-ally <25 % and peak mitral velocity <15 %, whereas withtamponade the variation is much greater.Echo is the investigation of choice in suspected cardiac

tamponade, with the diagnosis generally easy to makewhen aligned with clinical findings. It also assists withurgent pericardiocentesis.

Fig. 4 Examples of assessing the shocked patient using spectral Doppler

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Dynamic LVOT obstructionThe true incidence of dynamic left ventricular outflowobstruction in critically ill patients is unknown. It re-quires advanced echo Doppler expertise and in the pasthas usually gone unrecognized. Left ventricular wallhypertrophy classically has alerted the clinician to thepossibility of hypertrophic obstructive cardiomyopathyand searching for LVOT obstruction would be seen asstandard practice.Dynamic LVOT obstruction can be present in the

aged ambulatory population in the absence of wallhypertrophy [51]. Factors that make the critically illpopulation more susceptible, apart from age, includetachycardia, hypovolemia, and inotropes [52, 53]. 2Decho examination reveals close approximation of lateralwall and septum, plus systolic anterior motion of the an-terior mitral leaflet. TEE examination often supplementsthe TTE approach. Color Doppler will reveal turbulentflow through the LVOT with continuous wave Dopplerpicking up high velocities indicating obstructive and sub-sequent pulsed-wave Doppler identifying exactly wherethat obstruction occurs. A classic spectral Doppler patternis the so‐called “dagger” shape LVOT flow. Treatment in-cludes re‐establishing an adequate intravascular volume,reducing heart rate to enhance diastolic filling time, andceasing inotropes (Fig. 4).

Septic shockA variety of cardiac changes can be associated with septicshock, although a normal study also is not unusual(Table 2). Abnormalities in left ventricular systolic func-tion, left ventricular diastolic function, and right ventricu-lar function have all been described [54]. Contractileimpairment may be exhibited as specific patterns such asseen in Takutsubo syndrome with apical akinesis andballooning accompanied by good basal left ventricularcontraction. Occasionally, LVOT obstruction is also de-scribed [55].A variety of patterns can occur in septic cardio-

myopathy, including global left and/or right ventricular

hypokinesis, left ventricular segmental wall motion de-fect patterns, and subtle changes only identified on sen-sitive examination, such as with speckle tracking usingglobal longitudinal strain [56]. Importantly, the contract-ile dysfunction is almost always reversible over days,unless concomitant underlying coronary artery diseaseor myocarditis are present. Measurement of ventricularpreload using echo to optimize a fluid managementstrategy is recommended. A major pathological contri-bution to shock in sepsis is peripheral vasoplegia and al-though this is not measurable with echo, the cardiacfindings can be taken into account when estimating it.For example, in shock a hyperdynamic, well filled leftventricle is usually a clue to the presence of marked per-ipheral vasodilatation. Echo has a pertinent role in evalu-ating the valves in septic shock, both structurally andfunctionally. Endocarditis or peri‐valvular abscesses maybe the cause of shock. TEE is the preferred technique,although TTE can still be valuable in the acute setting.The severity of any valve functional abnormality needsto be assessed and more expert examination soughtwhere necessary, especially where prosthetic valves orcongenital heart disease exist.

Other causes of shockAnaphylactic, neurogenic, hypo‐adrenalism, and otherless common causes of shock will be assisted by the ap-plication of urgent echocardiography, sometimes indirecting the clinician away from the heart as a cause ofshock in the presence of a normal study.

ConclusionsEchocardiography is perhaps the most single useful toolin the diagnosis and management of shock, particularlywhere the etiology is undifferentiated or multifactorial.Non‐invasive and rapid to initiate, it can be applied atthe bedside anytime during the day or night. An initialbasic or RACE study can lead to commencement oftreatment, with a more advanced study subsequentlyproviding incremental and vital additional information.

AcknowledgementsI would like to express gratitude and appreciation to Professor StephenHuang for advice on the content and Ms Novea Riley for secretarialassistance in the preparation of this manuscript.

Author’s contributionAM designed and wrote the manuscript as the sole author.

Competing interestsThe author declares that he has no competing interests.

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Table 2 Cardiac abnormalities in severe sepsis

Left ventricular dilatation

Left ventricular contraction impairment

Global

Segmental

Left ventricular diastolic dysfunction

Right ventricle systolic/diastolic dysfunction

Ventricular outflow obstruction

Valvular lesions

Functional

Endocarditis

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